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Suramin-Restricted Blood Volume in the Placenta of Normal and Diabetic Rats is Normalized by Vitamin E Treatment
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology. (Teratology)
2007 (English)In: Placenta, ISSN 0143-4004, E-ISSN 1532-3102, Vol. 28, no 5-6, 505-515 p.Article in journal (Refereed) Published
Abstract [en]

Previously maternal and fetal alterations resembling human pre-eclampsia were induced in pregnant rats by injections of the angiogenesis inhibitor Suramin. These alterations were aggravated by maternal diabetes and partly rectified by vitamin E supplementation. In the present study we evaluated the morphology of placentae and kidneys in this model. Non-diabetic and streptozotocin-induced diabetic pregnant rats of two rat strains (U and H) were treated with Suramin or saline, and given standard or vitamin E-enriched food. On gestational day 20 one placenta and the left kidney of the mother were collected for morphological and stereological analysis. In the placental trophospongium Suramin treatment caused cysts, which were further enhanced by maternal diabetes. Vitamin E treatment had no effect on the vacuolization. In the placental labyrinth of the non-diabetic rats Suramin treatment restricted maternal placental blood volume and increased the interface between maternal and fetal circulation. These changes were reversed by vitamin E treatment. Diabetes increased slightly the interface between the circulations in both rat strains. Suramin treatment decreased the interface, and vitamin E further decreased the interface in the diabetic U rats, whereas neither treatment affected the maternal-fetal interface in the diabetic H rats. The kidneys of Suramin-treated and diabetic rats were heavier compared to controls. Suramin treatment and maternal diabetes damaged renal glomeruli to a similar extent. Vitamin E treatment diminished the Suramin- and diabetes-induced glomerular damage in U rats, but not in H rats. The average cell count per glomerulus was decreased by Suramin in the U rats. Vitamin E treatment did not affect cell number per glomerulus in any group. We conclude that Suramin-injected pregnant rats constitute a valid animal model for placental dysfunction and pre-eclampsia, also from the histological perspective. The present work supports the notion that one important effect of untreated maternal diabetes may be impaired placentation, leading to oxidative stress, morphological damage, and compromised placental function.

Place, publisher, year, edition, pages
2007. Vol. 28, no 5-6, 505-515 p.
Keyword [en]
Placenta, Kidney, Suramin, Morphology, Diabetes, Vitamin E, Experimental pre-eclampsia, Rat
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-95575DOI: 10.1016/j.placenta.2006.06.015ISI: 000246449700018PubMedID: 16920189OAI: oai:DiVA.org:uu-95575DiVA: diva2:169850
Available from: 2007-03-23 Created: 2007-03-23 Last updated: 2017-12-14Bibliographically approved
In thesis
1. Experimental and Clinical Studies of Oxidative Stress in Pre-Eclampsia
Open this publication in new window or tab >>Experimental and Clinical Studies of Oxidative Stress in Pre-Eclampsia
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Impaired placentation and oxidative stress are proposed to play major roles in the pathogenesis of pre-eclampsia (PE). It has recently been pointed out that PE might be more than one disease and may have several different pathogeneses. This thesis describes a new animal model for PE and examines the role of oxidative stress in early respective late onset PE.

The effects of Suramin injections on day 10 and 11 of pregnancy were investigated in normal and diabetic rats of two strains (U and H), with or without additional vitamin E treatment. Suramin caused placental dysfunction in both rat strains: foetal growth restriction, increased resorption rate, reduced placental blood flow, and decreased maternal blood volume in the placenta. In the U strain Suramin also caused maternal hypertension and reduced renal blood flow. Oxidative stress in the Suramin treated rats was indicated by increased levels of isoprostane 8-iso-PGF in the placenta. Antioxidative treatment with vitamin E partly protected against the effects of Suramin. Streptozotocin-induced diabetes seemed to cause similar placental effects as Suramin, and in the diabetic rats the additional effects of Suramin were only moderate. In conclusion, Suramin-injected pregnant rats constitute a valid animal model for placental dysfunction (U and H rats) and PE (U rats).

Oxidative stress was estimated in women with early onset (≤ 32 weeks) or late onset (≥ 35 weeks) PE, in normotensive pregnant women of respective gestational length, and in healthy non-pregnant women. The ratio of PAI-1/PAI-2 was measured in serum, and the amount of isoprostane 8-iso-PGF was measured in placenta, serum, and urine. The ratio of PAI-1/PAI-2 and placental isoprostane levels were higher in women with early onset PE compared with all other groups. Serum levels of isoprostane were similar between groups. Urinary levels of isoprostane were similar in all pregnant women, but lower in non-pregnant women. These data indicate that pregnancy increases general oxidative stress, and that early onset, but not late onset PE, causes increased oxidative stress also in placental tissue. The pathogeneses of early and late onset PE are, therefore, not likely to be identical.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2007. 63 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 238
Keyword
Obstetrics and gynaecology, Pre-eclampsia, Oxidative stress, Diabetes, Placenta, Rat, Antioxidants, Suramin, Vitamin E, Vitamin C, PAI-1, PAI-2, Obstetrik och kvinnosjukdomar
Identifiers
urn:nbn:se:uu:diva-7717 (URN)978-91-554-6826-2 (ISBN)
Public defence
2007-04-13, B 21, Biomedicinskt centrum, Uppsala, 13:15
Opponent
Supervisors
Available from: 2007-03-23 Created: 2007-03-23 Last updated: 2013-08-30Bibliographically approved

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